CHOLINERGIC STIMULATION of the rostral part of the pontine reticular formation induces rapid-eye-movement (REM) sleep with atonia in intact animals, and lesions at this pontine site cause REM sleep without atonia.1,2,3 REM sleep without atonia

pontine reticular formation induces rapid-eye-movement (REM) sleep with atonia in intact animals, and lesions at this pontine site cause REM sleep without atonia.1,2,3 REM sleep without atonia is also induced by lesions in the medial medulla.4,5 In the decerebrate cat, both chemical and electrical stimulation delivered to the pontine inhibitory regions, as well as to portions of the medial medulla, produce a collapse of decerebrate rigidity.6 The latency to the onset of pontine-induced muscle tone suppression is longer than that elicited by medullary stimulation in the decerebrate cat.7-9 Descending pathways that originate in the mesopontine reticular formation and project to the medullary inhibitory region10,11 appear to mediate atonia. However, atonia is much more difficult to elicit by medullary stimulation in cats transected at the pontomedullary junction than in cats transected at the midbrain level.12 Also, chronically maintained medullary cats never have periods of atonia.13 These findings suggest that the pons may contribute to atonia elicited by medullary stimulation. In the current study, we have reversibly inactivated the pontine reticular formation by means of lidocaine microinjection. The degree of medullary-induced muscle tone suppression was assessed before and after microinjection of lidocaine. In prior studies, we identified ventral medullary sites at which 500-msec stimulation produced a suppression of muscle tone.6 These sites correspond to the medullary inhibitory area identified by Magoun and Rhines14 with electrical stimulation. We found that activation of nonNMDA glutamate receptors at medullary inhibitory sites in the rostral medulla produced inhibition, and that blockade of these nonNMDA glutamate receptors reversed muscle atonia elicited by microinjection of agonists into the pontine reticular formation.8 We found that the caudomedial medullary atonia sites identified by electrical stim-